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Other Names for L-Dopa
Safe and effective dosage for L-DOPA is said to be anywhere from 100 mg to 900 mg per day. In this range the affects you experience could be mild or very pronounced. Every individual has different sensitivity to L-DOPA so it is recommended to start with low doses and gradually increase the dosage in increments of 100 mg. Dosages at 100 mg research has shown that it is ineffective at increasing libido or sexual arousal (1). However, case studies of persons consuming dosages that exceed 2.5 g have resulted in hypersexuality and frequent erections (2).
As a dietary supplement, L- DOPA is frequently sources from velvet bean (mucuna puriens) which naturally contains 3-7% by weight (6).
L-DOPA is a neurotransmitter precursor to dopamine made and used in normal human biology and in some plants and animals. Humans obtain L-DOPA from through biosynthesis from the amino acid L-tyrosine, with the help of tyrosine hydroxylase. L-DOPA is the precursor to the neurotransmitters norepinephrine, dopamine, and epinephrine which are collectively acknowledged as catecholamines.
L-DOPA was first isolated around 1910 from the seedlings of vicia faba. L-dopa decarboxylase was then discovered in 1938, which is an enzyme that transforms L-DOPA into dopamine.
In 1957 dopamine was found to occur in the brain, and in 1959 it was shown to be enriched in a specific part of the brain. Postmortem studies conducted in 1960 showed that dopamine deficiency correlated with Parkinson’s disease, which provided a basis for dopamine replacement therapy using L-DOPA (4). The first successful clinical trial with L-DOPA was carried out in 1961, and in 1967 L-DOPA was introduced as a treatment for Parkinson’s disease.
Oral availability for L-DOPA increases with chronic administration (7). Levodopa is sometimes co-administered with a peripheral Dopa decarboxylase inhibitor to prevent excess dopamine in the peripheral nervous system. Additionally vitamin B6 is occasionally co-administered with L-DOPA as pyridoxine is required for dopa-decarboxlyase to function.
L-DOPA’s Method of Action
As A Dopamine Precursor
When L-DOPA is orally consumed it is able to cross the blood brain barrier and is converted to into dopamine with the help of DOPA decarboxylase. The dopamine then immediately relays messages to nerve cells which govern arousal and pleasure responses. It then stimulates the release of hormonal neurotransmitters in the pituitary gland and hypothalamus. These include norepinephrine and epinephrine which increase metabolism and boost energy.
L-DOPA is an effective dopamine precursor as dopamine itself does not cross the blood-brain barrier, which means it cannot be used to support brain dopamine levels. L-dopa does gain access to the brain where it is converted into dopamine to restore the brains dopamine deficiency, it does enable normal body movements allowing people with the disease to stay functional for longer periods of time and reduces the symptoms of Parkinson’s disease (4).
Hormones and Libido
In rodents, a high dose of L-DOPA is associated with increased testosterone within 1-2 weeks which may be due to elevated luteinizing hormone. Two human studies have demonstrated L-dopa is able to increase growth hormone shortly after administration (9) (10).
Dopamine’s role in libido is well established, and there’s a theoretical possibility of enhanced libido following L-DOPA’s consumption, indeed a side effect of high dose L-DOPA is hyper sexuality (11). Research involving healthy men and women showed 100mg of L-DOPA was unable to enhance libibo, however motor response to sexual stimuli was enhanced in men, but not women (12).
Enhanced Word Learning In Healthy Individuals
One clinical study looked at L-DOPA’s effect on memory. 40 healthy adult participants were assigned to 100mg L-DOPA or placebo for 5 days, during which the subjects were exposed to a variety of unfamiliar words. The researchers concluded levodopa enhanced the speed and long term retention of the learned words compared to placebo (8).
A common side effect when L-DOPA is used for treating Parkinson’s disease is abnormal motor control (5). Loss of dopamine in the basal ganglia is associated with dyskinogenesis, the involuntary movement of the skeletal muscles (5). The likelihood of healthy persons experiencing dyskinesia is unknown, but the chance of it happening appears to rise with disease pathology.